溃疡性结肠炎是一种最常见的慢性炎症性疾病，危害极大。我们发现新的分泌蛋白FAM96A在DSS诱导的结肠炎动物模型中具有明确的保护作用。Fam96a-/-鼠结肠炎症状明显加重，转基因鼠症状减轻。rhFAM96A对结肠炎具有保护作用。该项目是研究FAM96A参与肠道区域免疫调节和在结肠炎中作用机制。研究FAM96A在肠道区域免疫组织和各类细胞中表达分布特点；FAM96A对肠道粘膜上皮细胞、固有淋巴样细胞、巨噬细胞和DC的作用；寻找、确定FAM96A的靶细胞和受体，研究FAM96A调控IL-23和IL-22表达机制，研究FAM96A的信号转导通路，最终阐明FAM96A如何通过对肠道区域的免疫调节而对结肠炎起到了保护作用。通过该研究可以阐释FAM96A对肠道区域免疫的作用，对丰富肠道区域免疫的理论是一个重要的补充；确定FAM96A的靶细胞和受体可以对结肠炎提供新的治疗思路，有潜在的应用前景。

Ulcerative colitis(UC) is a most common chronic inflammatory desease which is caused by intestinal local immunity disorders. UC causes a ruinous disaster and people haven’t realized its definite mechanism. We have identified a novel secretory protein FAM96A ,which played an important part in DSS induced colitis model. Fam96a knock-out mice showed more evident symptom, while FAM96A transgenic mice displayed reduced impairment.rhFAM96A was also protective in the model .We hope to study the mechanism for the regulatory role of FAM96A in intestinal local immunity, to study the its distribution in intestinal local immune tissues and different cells; to figure out its function on mucous epithelia ,ILCs, macrophages and DCs ;to find out and identify its target cells and receptor; to study the mechanisms for its regulation of IL-23 and IL-22 expression;to study its complicated signal pathway; Ultimately,we will clarify the definite mechanism of the protective function FAM96A exerts via regulation of intestinal local immunity.. Our research will elucidate the role of FAM96A in intestinal local immunity, which is an important supplement for current intestinal local immunity theory; identification of FAM96A target cells and receptor may provide a novel therapeutic way,and has potential application prospects .